Relevant bibliographies by topics / Brainstem hypoglossal motoneurons

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  2. Dissertations / Theses

Academic literature on the topic 'Brainstem hypoglossal motoneurons'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Brainstem hypoglossal motoneurons"

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Cifra, Alessandra, Francesca Nani, Elina Sharifullina, and Andrea Nistri. "A repertoire of rhythmic bursting produced by hypoglossal motoneurons in physiological and pathological conditions." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1529 (September 12, 2009): 2493–500. http://dx.doi.org/10.1098/rstb.2009.0071.

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The brainstem nucleus hypoglossus contains motoneurons that provide the exclusive motor nerve supply to the tongue. In addition to voluntary tongue movements, tongue muscles rhythmically contract during a wide range of physiological activities, such as respiration, swallowing, chewing and sucking. Hypoglossal motoneurons are destroyed early in amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease often associated with a deficit in the transport system of the neurotransmitter glutamate. The present study shows how periodic electrical discharges of motoneurons are mainly produced by a neuronal network that drives them into bursting mode via glutamatergic excitatory synapses. Burst activity is, however, modulated by the intrinsic properties of motoneurons that collectively synchronize their discharges via gap junctions to create ‘group bursters’. When glial uptake of glutamate is blocked, a distinct form of pathological bursting spontaneously emerges and leads to motoneuron death. Conversely, H 2 O 2 -induced oxidative stress strongly increases motoneuron excitability without eliciting bursting. Riluzole (the only drug currently licensed for the treatment of ALS) suppresses bursting of hypoglossal motoneurons caused by blockage of glutamate uptake and limits motoneuron death. These findings highlight how different patterns of electrical oscillations of brainstem motoneurons underpin not only certain physiological activities, but also motoneuron death induced by glutamate transporter impairment.
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Silva-Hucha, Silvia, Angel M. Pastor, and Sara Morcuende. "Neuroprotective Effect of Vascular Endothelial Growth Factor on Motoneurons of the Oculomotor System." International Journal of Molecular Sciences 22, no. 2 (January 15, 2021): 814. http://dx.doi.org/10.3390/ijms22020814.

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Vascular endothelial growth factor (VEGF) was initially characterized as a potent angiogenic factor based on its activity on the vascular system. However, it is now well established that VEGF also plays a crucial role as a neuroprotective factor in the nervous system. A deficit of VEGF has been related to motoneuronal degeneration, such as that occurring in amyotrophic lateral sclerosis (ALS). Strikingly, motoneurons of the oculomotor system show lesser vulnerability to neurodegeneration in ALS compared to other motoneurons. These motoneurons presented higher amounts of VEGF and its receptor Flk-1 than other brainstem pools. That higher VEGF level could be due to an enhanced retrograde input from their target muscles, but it can also be produced by the motoneurons themselves and act in an autocrine way. By contrast, VEGF’s paracrine supply from the vicinity cells, such as glial cells, seems to represent a minor source of VEGF for brainstem motoneurons. In addition, ocular motoneurons experiment an increase in VEGF and Flk-1 level in response to axotomy, not observed in facial or hypoglossal motoneurons. Therefore, in this review, we summarize the differences in VEGF availability that could contribute to the higher resistance of extraocular motoneurons to injury and neurodegenerative diseases.
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Robinson, David W., and William E. Cameron. "Time-Dependent Changes in Input Resistance of Rat Hypoglossal Motoneurons Associated with Whole-Cell Recording." Journal of Neurophysiology 83, no. 5 (May 1, 2000): 3160–64. http://dx.doi.org/10.1152/jn.2000.83.5.3160.

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The effect of cellular dialysis associated with whole-cell recording was studied in 24 developing hypoglossal motoneurons in a rat brainstem slice preparation. In all cases, establishing whole-cell continuity with the electrode solution resulted in an increase in the input resistance measured in current clamp. The mean magnitude of this increase was 39.7% and the time course of the maximum effect was quite variable. There was no correlation found between the time to maximum effect and the magnitude of the increase in resistance. These data indicate that the passive membrane properties are not constant during whole-cell recording in mammalian motoneurons.
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Sawczuk, A., and K. M. Mosier. "Neural Control of Tongue Movement With Respect To Respiration and Swallowing." Critical Reviews in Oral Biology & Medicine 12, no. 1 (January 2001): 18–37. http://dx.doi.org/10.1177/10454411010120010101.

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The tongue must move with remarkable speed and precision between multiple orofacial motor behaviors that are executed virtually simultaneously. Our present understanding of these highly integrated relationships has been limited by their complexity. Recent research indicates that the tongue's contribution to complex orofacial movements is much greater than previously thought. The purpose of this paper is to review the neural control of tongue movement and relate it to complex orofacial behaviors. Particular attention will be given to the interaction of tongue movement with respiration and swallowing, because the morbidity and mortality associated with these relationships make this a primary focus of many current investigations. This review will begin with a discussion of peripheral tongue muscle and nerve physiology that will include new data on tongue contractile properties. Other relevant peripheral oral cavity and oropharyngeal neurophysiology will also be discussed. Much of the review will focus on brainstem control of tongue movement and modulation by neurons that control swallowing and respiration, because it is in the brainstem that orofacial motor behaviors sort themselves out from their common peripheral structures. There is abundant evidence indicating that the neural control of protrusive tongue movement by motoneurons in the ventral hypoglossal nucleus is modulated by respiratory neurons that control inspiratory drive. Yet, little is known of hypoglossal motoneuron modulation by neurons controlling swallowing or other complex movements. There is evidence, however, suggesting that functional segregation of respiration and swallowing within the brainstem is reflected in somatotopy within the hypoglossal nucleus. Also, subtle changes in the neural control of tongue movement may signal the transition between respiration and swallowing. The final section of this review will focus on the cortical integration of tongue movement with complex orofacial movements. This section will conclude with a discussion of the functional and clinical significance of cortical control with respect to recent advances in our understanding of the peripheral and brainstem physiology of tongue movement.
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5

Powell, Gregory L., Richard B. Levine, Amanda M. Frazier, and Ralph F. Fregosi. "Influence of developmental nicotine exposure on spike-timing precision and reliability in hypoglossal motoneurons." Journal of Neurophysiology 113, no. 6 (March 15, 2015): 1862–72. http://dx.doi.org/10.1152/jn.00838.2014.

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Smoothly graded muscle contractions depend in part on the precision and reliability of motoneuron action potential generation. Whether or not a motoneuron generates spikes precisely and reliably depends on both its intrinsic membrane properties and the nature of the synaptic input that it receives. Factors that perturb neuronal intrinsic properties and/or synaptic drive may compromise the temporal precision and the reliability of action potential generation. We have previously shown that developmental nicotine exposure (DNE) alters intrinsic properties and synaptic transmission in hypoglossal motoneurons (XIIMNs). Here we show that the effects of DNE also include alterations in spike-timing precision and reliability, and spike-frequency adaptation, in response to sinusoidal current injection. Current-clamp experiments in brainstem slices from neonatal rats show that DNE lowers the threshold for spike generation but increases the variability of spike-timing mechanisms. DNE is also associated with an increase in spike-frequency adaptation and reductions in both peak and steady-state firing rate in response to brief, square wave current injections. Taken together, our data indicate that DNE causes significant alterations in the input-output efficiency of XIIMNs. These alterations may play a role in the increased frequency of obstructive apneas and altered suckling strength and coordination observed in nicotine-exposed neonatal humans.
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Allain, Anne-Emilie, Hervé Le Corronc, Alain Delpy, William Cazenave, Pierre Meyrand, Pascal Legendre, and Pascal Branchereau. "Maturation of the GABAergic Transmission in Normal and Pathologic Motoneurons." Neural Plasticity 2011 (2011): 1–13. http://dx.doi.org/10.1155/2011/905624.

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γ-aminobutyric acid (GABA) acting on Cl−-permeable ionotropic type A (GABAA) receptors (GABAAR) is the major inhibitory neurotransmitter in the adult central nervous system of vertebrates. In immature brain structures, GABA exerts depolarizing effects mostly contributing to the expression of spontaneous activities that are instructive for the construction of neural networks but GABA also acts as a potent trophic factor. In the present paper, we concentrate on brainstem and spinal motoneurons that are largely targeted by GABAergic interneurons, and we bring together data on the switch from excitatory to inhibitory effects of GABA, on the maturation of the GABAergic system and GABAAR subunits. We finally discuss the role of GABA and its GABAAR in immature hypoglossal motoneurons of the spastic (SPA) mouse, a model of human hyperekplexic syndrome.
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7

Nakajima, Misuzu. "Brainstem Segmental Arrangement of Sucking Rhythm Generators for Trigeminal, Facial and Hypoglossal Motoneurons." JOURNAL OF THE STOMATOLOGICAL SOCIETY,JAPAN 66, no. 1 (1999): 88–97. http://dx.doi.org/10.5357/koubyou.66.88.

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8

Fietkiewicz, Christopher, Kenneth A. Loparo, and Christopher G. Wilson. "Drive latencies in hypoglossal motoneurons indicate developmental change in the brainstem respiratory network." Journal of Neural Engineering 8, no. 6 (October 1, 2011): 065011. http://dx.doi.org/10.1088/1741-2560/8/6/065011.

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9

Komarov, M., M. Naji, G. Krishnan, A. Malhotra, F. Powell, I. Rukhadze, V. Fenik, and M. Bazhenov. "0139 COMPUTATIONAL MODEL OF BRAINSTEM CIRCUIT FOR STATE-DEPENDENT CONTROL OF HYPOGLOSSAL MOTONEURONS." Sleep 40, suppl_1 (April 28, 2017): A52. http://dx.doi.org/10.1093/sleepj/zsx050.138.

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Lape, Remigijus, and Andrea Nistri. "Characteristics of fast Na+current of hypoglossal motoneurons in a rat brainstem slice preparation." European Journal of Neuroscience 13, no. 4 (February 2001): 763–72. http://dx.doi.org/10.1046/j.0953-816x.2000.01433.x.

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Dissertations / Theses on the topic "Brainstem hypoglossal motoneurons"

1

Cifra, Alessandra. "Hypoglossal motoneurons: a model to investigate physiological and pathophysiological properties of brainstem motoneurons." Doctoral thesis, SISSA, 2011. http://hdl.handle.net/20.500.11767/4781.

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Hypoglossal motoneurons (HMs) are brainstem neurons that command rhytmic contraction of the tongue muscles during breathing as well as a variety of non-respiratory functions such as sleep, vocalization, suckling and swallowing. Neurodegenerative diseases like amyotrophic lateral sclerosis (ALS; Lou-Gehrig disease) often damage HMs with distressing symptoms like dysarthria, dysphagia and breathing failure...
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Wollman, Lila Buls, and Lila Buls Wollman. "Plasticity of Brainstem Motor Systems in Response to Developmental Nicotine Exposure." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/626307.

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Developmental nicotine exposure (DNE) is known to cause abnormal development of multiple brain regions and results in impaired control of breathing and altered behaviors that rely on proper coordination of the muscles of the tongue. The adverse effects of nicotine are presumably caused by its actions on nicotinic acetylcholine receptors (nAChRs), which modulate fast-synaptic transmission and play a prominent role during brain development. Previous work has shown that DNE alters nAChR function in multiple brainstem regions (Pilarski et al., 2012, Wollman et al, 2016). Moreover, DNE causes multiple changes to XIIMNs, which innervate the muscles of the tongue (Powell et al., 2016, Powell et al., 2015, Pilarski et al., 2011). These changes likely reflect both altered development as a primary outcome of the chronic presence of nicotine, as well as, homeostatic adjustments made in an attempt to maintain normal motoneuron output. With the experiments described here, we tested the hypothesis that DNE alters the development of fast-synaptic transmission to XIIMNs, which, along with intrinsic properties of these neurons, is a main determinant of motor output to the muscles of the tongue. Additionally, we tested the hypothesis that DNE alters the function of nAChRs located on multiple brainstem neurons, including those that modulate fast-synaptic transmission to XIIMNs. For these experiments, we used whole cell patch clamp recordings from XIIMNs in a transverse slice of the medulla, and extracellular recordings from the 4th cervical ventral root in the brainstem spinal cord, split bath preparation. All preparations were obtained from control or DNE neonatal rats in the first week of life. Overall, the results of these experiments show that DNE alters fast-synaptic transmission to XIIMNs, which likely reflects appropriate homeostatic adjustments aimed at maintaining normal motor output at rest. However, these results also show that nAChR function is significantly altered by DNE, indicating fast-synaptic transmission may not be appropriately modulated in response to increased release of acetylcholine (ACh), the endogenous neurotransmitter for nAChRs.
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Charifoullina, Elina. "Oscillatory motor discharges by brainstem neurons: functional mechanisms and consequences for cell survival." Doctoral thesis, SISSA, 2006. http://hdl.handle.net/20.500.11767/4671.

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